ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
The carboxy-terminal fragment of inhibitor-2 of protein phosphatase-2A induces Alzheimer disease pathology and cognitive impairment.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 79 citations in OpenAlex.
- Amyloid-β and Tau in Alzheimer's disease: pathogenesis, mechanisms, and interplay.Cell death & disease · 2026Review
- PP2A methylesterase, PME-1, and PP2A methyltransferase, LCMT-1, control sensitivity to impairments caused by injury-related oligomeric tau.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Astrocytes distress triggers brain pathology through induction of δ secretase in a murine model of Alzheimer's disease.Nature communications · 2025Article
- The impact of sodium nitrite and intermittent fasting on neurofilament and tau protein phosphorylation, and spatial learning in rat hippocampus.Experimental brain research · 2024Article
- The next decade of SET: from an oncoprotein to beyond.Journal of molecular cell biology · 2024Review
- Article
- Thirty years of SET/TAF1β/I2PP2A: from the identification of the biological functions to its implications in cancer and Alzheimer's disease.Bioscience reports · 2022Review
- A delta-secretase-truncated APP fragment activates CEBPB, mediating Alzheimer's disease pathologies.Brain : a journal of neurology · 2021Article
- Leucine Carboxyl Methyltransferase 1 Overexpression Protects Against Cognitive and Electrophysiological Impairments in Tg2576 APP Transgenic Mice.Journal of Alzheimer's disease : JAD · 2021Article
- Protein Biomarkers for the Diagnosis of Alzheimer's Disease at Different Stages of Neurodegeneration.International journal of molecular sciences · 2020Review
- Reduced Expression of the PP2A Methylesterase, PME-1, or the PP2A Methyltransferase, LCMT-1, Alters Sensitivity to Beta-Amyloid-Induced Cognitive and Electrophysiological Impairments in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Axonal Degeneration in AD: The Contribution of Aβ and Tau.Frontiers in aging neuroscience · 2020Review
- GSK-3β and ERK1/2 incongruously act in tau hyperphosphorylation in SPS-induced PTSD rats.Aging · 2019Article
- Rac1 activation links tau hyperphosphorylation and Aβ dysmetabolism in Alzheimer's disease.Acta neuropathologica communications · 2018Article
- Article
- Untangling Tau and Iron: Exploring the Interaction Between Iron and Tau in Neurodegeneration.Frontiers in molecular neuroscience · 2018Review
- Involvement of Activation of Asparaginyl Endopeptidase in Tau Hyperphosphorylation in Repetitive Mild Traumatic Brain Injury.Journal of Alzheimer's disease : JAD · 2018Article
- Regulation of SET Gene Expression by NFkB.Molecular neurobiology · 2017Article
- Sex Differences in the Cognitive and Hippocampal Effects of Streptozotocin in an Animal Model of Sporadic AD.Frontiers in aging neuroscience · 2017Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Development of rational therapeutic treatments of Alzheimer disease (AD) requires the elucidation of the etiopathogenic mechanisms of neurofibrillary degeneration and β-amyloidosis, the two hallmarks of this disease. Here we show, employing an adeno-associated virus serotype 1 (AAV1)-induced expression of the C-terminal fragment (I(2CTF)) of I(2)(PP2A), also called SET, in rat brain, decrease in protein phosphatase 2A (PP2A) activity, abnormal hyperphosphorylation of tau, and neurodegeneration; littermates treated identically but with vector only, i.e., AAV1-enhanced green fluorescent protein (GFP), served as a control. Furthermore, there was an increase in the level of activated glycogen synthase kinase-3β and enhanced expression of intraneuronal Aβ in AAV1-I(2CTF) animals. Morris water maze behavioral test revealed that infection with AAV1-I(2CTF) induced spatial reference memory and memory consolidation deficits and a decrease in the brain level of pSer133-CREB. These findings suggest a novel etiopathogenic mechanism of AD, which is initiated by the cleavage of I(2)(PP2A), producing I(2CTF), and describe a novel disease-relevant nontransgenic animal model of AD.
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